Document Detail

Ventilatory and cardiovascular responses to hypercapnia and hypoxia in multiple-system atrophy.
MedLine Citation:
PMID:  20142529     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Loss of medullary sympathoexcitatory neurons may contribute to baroreflex failure, leading to orthostatic hypotension in multiple-system atrophy (MSA). The cardiovascular responses to chemoreflex activation in MSA have not been explored to date.
OBJECTIVES: To determine whether ventilatory and cardiovascular responses to hypercapnia and hypoxia during wakefulness are systematically impaired in MSA.
DESIGN: Case-control study.
SETTING: Mayo Clinic, Rochester, Minnesota.
PATIENTS: Sixteen patients with probable MSA (cases) and 14 age-matched control subjects (controls).
MAIN OUTCOME MEASURES: Minute ventilation, blood pressure, and heart rate responses to hypercapnia and hypoxia during wakefulness. Hypercapnia was induced by a rebreathing technique and was limited to a maximal expiratory partial pressure of carbon dioxide of 65 mm Hg. Hypoxia was induced by a stepwise increase in inspiratory partial pressure of nitrogen and was limited to a minimal arterial oxygen saturation of 80%. Ventilatory responses were assessed as slopes of the regression line relating minute ventilation to changes in arterial oxygen saturation and partial pressure of carbon dioxide.
RESULTS: In cases, ventilatory responses to hypercapnia and hypoxia were preserved, despite the presence of severe autonomic failure, while cardiovascular responses to these stimuli were impaired. Among cases, hypercapnia elicited a less robust increase in arterial pressure than among controls, and hypoxia elicited a depressor response rather than the normal pressor responses (P < .001 for both).
CONCLUSIONS: Ventilatory responses to hypercapnia and hypoxia during wakefulness may be preserved in patients with MSA, despite the presence of autonomic failure and impaired cardiovascular responses to these stimuli. A critical number of chemosensitive medullary neurons may need to be lost before development of impaired automatic ventilation during wakefulness in MSA, whereas earlier loss of medullary sympathoexcitatory neurons may contribute to the impaired cardiovascular responses in these patients.
Axel Lipp; James D Schmelzer; Phillip A Low; Bruce D Johnson; Eduardo E Benarroch
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Archives of neurology     Volume:  67     ISSN:  1538-3687     ISO Abbreviation:  Arch. Neurol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-09     Completed Date:  2010-03-05     Revised Date:  2014-09-09    
Medline Journal Info:
Nlm Unique ID:  0372436     Medline TA:  Arch Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  211-6     Citation Subset:  AIM; IM    
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MeSH Terms
Anoxia / etiology*
Autonomic Nervous System Diseases / etiology
Blood Pressure / physiology*
Case-Control Studies
Heart Rate / physiology*
Hypercapnia / etiology*
Hypotension, Orthostatic / etiology
Middle Aged
Multiple System Atrophy / complications*
Pulmonary Ventilation / physiology*
Statistics, Nonparametric
Grant Support
NS32352-02/NS/NINDS NIH HHS; P50 NS032352/NS/NINDS NIH HHS; P50 NS032352-030002/NS/NINDS NIH HHS; P50 NS032352-040002/NS/NINDS NIH HHS; P50 NS032352-050002/NS/NINDS NIH HHS; P50 NS032352-06A10005/NS/NINDS NIH HHS; P50 NS032352-110005/NS/NINDS NIH HHS; P50 NS032352-140005/NS/NINDS NIH HHS; P50 NS032352-150005/NS/NINDS NIH HHS
Comment In:
Arch Neurol. 2010 Oct;67(10):1288   [PMID:  20937966 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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